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MSK/Derm > Vasculitis > Flashcards

Vasculitis Flashcards

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1
Q

What are the layers of arteries?

A

endothelium (tunica intima)

smooth muscle (tunica media)

fibrous connective tissue (tunica adventitia)

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2
Q

What are the types of vascular disease?

A

arterial diseases

venous diseases

lymphatic diseases

vascular tumors

congenital anomalies

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3
Q

What are the categories of arterial diseases?

A

arteriosclerosis

aneurysm

vasculitis

functional arterial disease

fibromuscular dysplasia

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4
Q

What is vasculitis?

A

inflammation of and damage to blood vessels

vessel damage leads to ischemia (usually predominates)** **or aneurysm which compromises end-organ function

heterogenous - many etiologies, many manifestations

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5
Q

What are causes of secondary vasculitis?

A

infection

drugs

malignancy

connective tissue disease (lupus or progressive systemic sclerosis)

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6
Q

What are do the primary vasculitides have in common?

A

autoimmune etiology

inflammation of the vessel wall often leads to necrosis or aneurysmal formation

vessel wall inflammation -> occlusion or aneurysm -> end organ dysfunction

constitutional symptoms (fever, weight loss, malaise, anorexia, fever)

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7
Q

What are the subclassifications of vasculitis?

A

large vessel

medium-sized vessel

small vessel

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8
Q

What are the large vessel vasculitis?

A

Giant Cell Arteritis

Takayasu’s Arteritis

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9
Q

What are the medium-sized vessel vasculitides?

A

Polyarteritis Nodosa

Kawasaki disease

Thromboangiitis Obliterans

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10
Q

What are the small vessel vasculitides?

A

Immune Complex Mediated

ANCA-associated

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11
Q

What is the classic presentation of giant cell arteritis (aka temporal arteritis)?

A

patients > 50 yrs, men more than women

extracranial arteries, temporal is common

classic presentation: fever, anemia, high ESR, headaches

other common manifestations:

  • jaw claudication
  • polymyalgia rheumatica (pain and stiffness in the hips and shoulders)
  • involvement of the ophthalmic artery can lead to blindness
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12
Q

How is the diagnosis of giant cell arteritis confirmed?

A

temporal artery biopsy

granulomatous inflammation - can see giant cells in vessel walls, which gives the arteritis its name

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13
Q

What is the treatment for giant cell arteritis?

A

high-dose steroids such as prednisone

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14
Q

What is the classic presentation of Takayasu’s Arteritis?

A

women < 50

asian descent

constitutional symptoms first (fever and weight loss) before clinical manifestation of clinical symptoms

involves ascending aorta and immediate branches

“pulseless disease” (decrease in peripheral pulse)

end-organ blood supply can also be affected (neurologic symptoms, claudication, or pulmonary hypertension)

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15
Q

What are the histological findings of Takayasu’s Arteritis?

A

histology is the same as temporal arteritis

giant cells are present

inflammation across all 3 layers of artery

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16
Q

What is the treatment for Takayasu’s Arteritis?

A

steroids

cytotoxic agents

anaotmic correction of stenosis - stents or bipass if needed

17
Q

What are the common clinical findings of Polyarteritis Nodosa?

A

often middle-aged patients

small-medium sized muscular arteries

skin manifestations such as cutaneous nodules

Mononeuritis Multiplex (people have peripheral neuropathies because of involvement of arteries associated with no central nerve identifiable)

Renal: hematuria

30% associated with Hep B

GI manifestations: abdominal pain

18
Q

What are the phases of Polyarteritis Nodosa?

A

acute phase - transmural inflammation and fibrinoid necrosis

chronic phase - fibrous wall thickening

stages can coexist!

19
Q

What is the treatment for Polyarteritis Nodosa?

A

corticosteroids and cyclophosphamide

20
Q

What is the common presentation of Kawasaki Disease?

A

young children (less than 4)

T-cell delayed hypersensitivity

endothelial antibodies precipitating acute vasculitis

Classic Pentad: fever, conjunctivitis, strawberry tongue, cervical lymphadenitis, desquamative rash

can lead to MI or death

21
Q

What are the risks of leaving Kawasaki Disease untreated?

A

risk of coronary artery ectasia and aneurysms

22
Q

What is the treatment for Kawasaki Disease?

A

high dose aspirin

100 mg/kg/day

intravenous immunoglobulin

23
Q

What are the general features of Thromboangiitis Obliterans (Buerger’s Disease)?

A

medium-small arteries

very cellular, inflammatory thrombus with relative vessel wall sparing

young heavily smoking males

can involve nerve and vein

very segmental - leads to symptoms of claudication

tibial and radial arteries most involved

can lead to rest limb pain, ulcerations, and gangrene

24
Q

What are the classic symptoms of Thromboangiitis Obliterans?

A

rest pain

instep claudication

Raynaud’s Phenomenon

Limb ischemia

superficial thrombophlebitis

25
Q

What is the treatment for thromboangiits obliterans?

A

stop smoking

likely that further artery involvement will cease

patients may still be left with claudication

26
Q

What is Raynaud’s Phenomenon?

A

triphasic change on cold exposure:

1) hyperemia (fingers turn red)
2) vasoconstriction (fingers blanch)
3) blue coloration from long-term tissue hypoxia

Primary - Raynaud’s disease if no cause

Secondary - Raynaud’s Phenomenon if secondary cause

27
Q

What is the treatment for Raynaud’s Phenomenon?

A

avoid cold exposure

calcium channel blockers

28
Q

What are the ANCA-associated small vessel vasculitides?

A

Granulomatosis with Polyangiitis (aka Wegener’s)

Microscopic Polyangiitis

Churg-Strauss Syndrome

29
Q

What is Henoch-Schonlein Purpura?

A

small vessels

children less than 10

IgA deposition in capillaries and venules

necrotising lesions

Palpable purpura - buttocks, lower extremities, and over extensor surfaces of arms and legs

Other symptoms:

  • polyarthralgia without arthritis
  • abdominal pin
  • renal involvement
  • often antecedent URI-type illness
30
Q

What is the treatment for Henoch-Schonlein Purpura?

A

usually self-resolving

steroids can help

prognosis is usually very good

31
Q

What is ANCA?

A

Antineutrophil Cytoplasmic Antibodies

can see in vasculitis and other autoimmune disorders

perinuclear ANCA (anti-myeloperoxidase, MPO) and cytoplasmic ANCA (anti-proteinase 3, PR3)

32
Q

What is granulomatosis with polyangiitis?

A

two pathologic hallmarks:

1) granuloma formation
2) necrotizing vasculitis of smalla rteries and veins

middle-age patients and associated with c-ANCA

33
Q

What is the classic triad of granulomatosis with polyangiitis?

A

initial phase: upper respiratory tract - mucosal ulcerations, frequent URIs, pain and purulent discharge, chronic necrotizing inflammation

chronic phase: Lower respiratory tract (hemoptysis, dyspnea, pleuritic pain) and renal involvement (glomerulonephritis)

34
Q

What is the treatment of granulomatosis with polyangiitis?

A

steroids or cyclophosphamide

35
Q

What are the features of microscopic polyangiitis?

A

small vessels

constitutional symptoms

major manifestation:

  • renal involvement (nephritic syndrome, often RPGN clinically)
  • pulmonary involvement (pulmonary capillaritis and diffuse alveolar hemorrhage)

p-ANCA pattern

36
Q

What is the presentation of Churg-Strauss Syndrome?

A

1 in a million

classic triad:

1) asthma, allergic rhinitis, nasal polyps
2) peripheral eosinophilia
3) vasculitis

p-ANCA present in ~50%

Other manifestations:

  • peripheral neuropathy: mononeuritis multiplex quite common
  • myocarditis from eosinophilic infiltrates
  • palpable purpura
  • renal involvement less common
37
Q

What is the treatment for Churg-Strauss Syndrome?

A

corticosteroids, cyclophosphamide

MSK/Derm (54 decks)

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